Catalytic and photoresponsive BiZ/CuxS heterojunctions with surface vacancies for the treatment of multidrug-resistant clinical biofilm-associated infections.

We report a one-pot facile synthesis of highly photoresponsive bovine serum albumin (BSA) templated bismuth-copper sulfide nanocomposites (BSA-BiZ/CuxS NCs, where BiZ represents in situ formed Bi2S3 and bismuth oxysulfides (BOS)). As-formed surface vacancies and BiZ/CuxS heterojunctions impart superior catalytic, photodynamic and photothermal properties. Upon near-infrared (NIR) irradiation, the BSA-BiZ/CuxS NCs exhibit broad-spectrum antibacterial activity, not only against standard multidrug-resistant (MDR) bacterial strains but also against clinically isolated MDR bacteria and their associated biofilms. The minimum inhibitory concentration of BSA-BiZ/CuxS NCs is 14-fold lower than that of BSA-CuxS NCs because their multiple heterojunctions and vacancies facilitated an amplified phototherapeutic response. As-prepared BSA-BiZ/CuxS NCs exhibited substantial biofilm inhibition (90%) and eradication (>75%) efficiency under NIR irradiation. Furthermore, MRSA-infected diabetic mice were immensely treated with BSA-BiZ/CuxS NCs coupled with NIR irradiation by destroying the mature biofilm on the wound site, which accelerated the wound healing process via collagen synthesis and epithelialization. We demonstrate that BSA-BiZ/CuxS NCs with superior antimicrobial activity and high biocompatibility hold great potential as an effective photosensitive agent for the treatment of biofilm-associated infections.

Incongruent Expression of Brain-Derived Neurotrophic Factor and Cortisol in Schizophrenia: Results from a Randomized Controlled Trial of Laughter Intervention.

OBJECTIVE: Schizophrenia has been associated with dysfunction of the hypothalamic-pituitary-adrenal axis. Furthermore, alterations in neurotrophic factors might contribute to the pathogenesis of schizophrenia. We aimed to evaluate the effects of a simulated laughter intervention on the levels of cortisol and BDNF and to determine whether the effects associated with simulated laughter could be sustained after discontinuation of the intervention. METHODS: In this randomized controlled study, patients with schizophrenia according to DSM-IV clinical criteria were randomly assigned to receive either 8-week-long simulated laughter intervention (n=32) or treatment-as-usual group (control group, n=27). The serum levels of BDNF and cortisol were measured at baseline, week 8, and four weeks after discontinuation (week 12) of the intervention program. RESULTS: After an 8-week simulated laughter intervention, the laughter group had significantly higher levels of BDNF; however, four weeks after discontinuation of the intervention, the levels of BDNF significantly dropped. Interestingly, the levels of cortisol did not change significantly at week 8, but they were significantly elevated at week 12. The levels of BDNF and cortisol in the control group did not change significantly between week 0 and week 8. CONCLUSION: These findings suggest that the simulated laughter intervention has an early effect on neurogenesis with a significant delayed effect on stress regulation in subjects with schizophrenia.

Protective effects of Liuwei dihuang water extracts on diabetic muscle atrophy.

BACKGROUND: Liuwei dihuang (LWDH), a widely used traditional Chinese herbal medicine, has been noticed for its potential on the improvement of diabetic complications including diabetic nephropathy and diabetic encephalopathy. However, whether LWDH can improve the effects of diabetic skeletal muscle atrophy has not yet been reported. PURPOSE: The present study aimed to investigate the protective effects and mechanisms of the water extract of Liuwei dihuang (LWDH-WE) on skeletal muscle in cellular and animal models of diabetic muscle atrophy. STUDY DESIGN: The muscle protective effects of LWDH-WE on diabetic muscle atrophy and weakness were examined in methylglyoxal (MG)-treated C2C12 myotubes and streptozotocin (STZ)-treated C57BL/6 mice, respectively. METHODS: C2C12 myoblasts were differentiated by differentiation medium to form myotube structures. C2C12 myotubes were pre-treated with LWDH-WE 1 h before MG treatment. Diabetic mice were induced by single intraperitoneal injection of STZ (150 mg/kg) in C57BL/6 mice. Cell viability was determined by MTT and LDH assays. Protein expressions were detected by western blots. Morphological changes of cells were observed by an inverted microscope. Mitochondria membrane potential and reactive oxygen species (ROS) production were measured by flow cytometry. Muscle strength was evaluated by measuring grip strength of mice. RESULTS: In C2C12 myotubes, LWDH-WE attenuated MG-induced cellular death and oxidative damage accompanied with improving mitochondrial membrane potential, inhibiting NADPH oxidase (Nox) activation, and ROS production. Moreover, LWDH-WE could attenuate MG-induced atrophy of C2C12 myotubes accompanied with regulating protein synthesis (IGF-1R, Akt, mTOR) and protein degradation (FoxO3a, atrogin-1, MuRF-1) signals. In STZ-induced diabetic mice, LWDH-WE improved body weight and skeletal muscle mass of mice. LWDH-WE also enhanced muscle strength of STZ-induced diabetic mice. Furthermore, LWDH-WE enhanced the improvement of insulin on gastrocnemius muscle mass and grip strength in STZ-treated mice. CONCLUSION: LWDH-WE possesses skeletal muscle protection via reducing oxidative damage and regulating protein synthesis and degradation pathways in MG-induced atrophy of C2C12 myotubes. We also reveal the novel protection of LWDH-WE against STZ-induced reduction of muscle mass and muscle strength in mice.

Functional identity of hypothalamic melanocortin neurons depends on Tbx3.

Heterogeneous populations of hypothalamic neurons orchestrate energy balance via the release of specific signatures of neuropeptides. However, how specific intracellular machinery controls peptidergic identities and function of individual hypothalamic neurons remains largely unknown. The transcription factor T-box 3 (Tbx3) is expressed in hypothalamic neurons sensing and governing energy status, whereas human TBX3 haploinsufficiency has been linked with obesity. Here, we demonstrate that loss of Tbx3 function in hypothalamic neurons causes weight gain and other metabolic disturbances by disrupting both the peptidergic identity and plasticity of Pomc/Cart and Agrp/Npy neurons. These alterations are observed after loss of Tbx3 in both immature hypothalamic neurons and terminally differentiated mouse neurons. We further establish the importance of Tbx3 for body weight regulation in Drosophila melanogaster and show that TBX3 is implicated in the differentiation of human embryonic stem cells into hypothalamic Pomc neurons. Our data indicate that Tbx3 directs the terminal specification of neurons as functional components of the melanocortin system and is required for maintaining their peptidergic identity. In summary, we report the discovery of a key mechanistic process underlying the functional heterogeneity of hypothalamic neurons governing body weight and systemic metabolism.

The novel protective effects of loganin against 1-methyl-4-phenylpyridinium-induced neurotoxicity: Enhancement of neurotrophic signaling, activation of IGF-1R/GLP-1R, and inhibition of RhoA/ROCK pathway.

Loganin, a major iridoid glycoside obtained from fruits of Cornus officinalis, possesses anti-inflammatory, antitumor, antidiabetic, and osteoporosis prevention effects. Loganin has been linked to neuroprotection in several models of neurodegeneration, including Parkinson's disease (PD). However, mechanisms underlying the neuroprotective effects of loganin are still mostly unknown. Here, we demonstrated the protective effects of loganin against PD mimetic toxin 1-methyl-4-phenylpyridinium (MPP+ ) and the important roles of insulin-like growth factor 1 receptor (IGF-1R) and glucagon-like peptide 1 receptor (GLP-1R) in the neuroprotective mechanisms of loganin. In primary mesencephalic neuronal cultures treated with or without MPP+ , loganin up-regulated expressions of neurotrophic signals including IGF-1R, GLP-1R, p-Akt, BDNF, and tyrosine hydroxylase. Loganin protected against MPP+ -induced apoptosis by up-regulating antiapoptotic protein and down-regulating proapoptotic protein. Moreover, loganin attenuated MPP+ -induced neurite damage via up-regulation of GAP43 and down-regulation of membrane-RhoA/ROCK2/p-LIMK/p-cofilin. Loganin also attenuated MPP+ -induced reactive oxygen species (ROS) production. However, both AG1024, an IGF-1R antagonist, and exendin 9-39, a GLP-1R antagonist, attenuated the protective effects of loganin on MPP+ -induced cytotoxicity, apoptosis, neurite length decrease, and ROS production. Our results suggest that loganin attenuates MPP+ -induced apoptotic death, neurite damage, and oxidative stress through enhancement of neurotrophic signaling, activation of IGF-1R/GLP-1R, and inhibition of RhoA/ROCK pathway, providing the evidence that loganin possesses novel neuroprotective effects.

Resveratrol prevents nanoparticles-induced inflammation and oxidative stress via downregulation of PKC-α and NADPH oxidase in lung epithelial A549 cells.

BACKGROUND: Exposure to carbon black nanoparticles (CBNPs), a well-known industrial production, promotes pulmonary toxicity through inflammation and oxidative stress. Recent studies show that some polyphenols exert their antioxidant properties through regulation of protein kinase C-α (PKC-α) and NADPH oxidase (Nox) signaling. Resveratrol, a dietary polyphenol in fruits, possesses various health beneficial effects including anti-inflammatory and antioxidative properties. In this study, we aimed to elucidate the involvement of PKC-α and Nox in CBNPs-induced inflammation and oxidative stress, and to investigate the protective effects of resveratrol on CBNP-induced inflammation and oxidative stress in human lung epithelial A549 cells. METHODS: The production of reactive oxygen species (ROS) and the change of mitochondrial membrane potential (ΔΨm) were measured by flow cytometry. Nitric oxide (NO) was measured using the Griess reagent, and prostaglandin E2 (PGE2) production was detected by ELISA, while protein expressions were measured by Western blotting analysis. RESULTS: In lung epithelial A549 cells, CBNPs significantly enhanced oxidative stress by upregulation of Nox2 and membrane expression of p67phox accompanied with increase of ROS production. CBNPs also increased inflammatory factors, including iNOS, COX-2, NO and PGE2. However, resveratrol attenuated the above effects induced by CBNPs in A549 cells; additionally, CBNPs-induced activation of PKC-α was observed. We found that PKC-α inhibitor (Gö6976) could attenuate CBNPs-induced inflammation by down-regulation of ROS, NO and PGE2 production in A549 cells, suggesting PKC-α might be involved in CBNPs-induced oxidative stress and inflammation. Our results also found resveratrol was able to inhibit protein expression of PKC-α induced by CBNPs. Moreover, ROS scavenger (NAC) and Nox inhibitor (DPI) attenuated CBNPs-induced expressions of iNOS and COX-2. DPI could also attenuate CBNPs-induced ROS, NO and PGE2 production. CONCLUSIONS: Resveratrol attenuated CBNPs-induced oxidative and inflammatory factors in lung epithelial A549 cells, at least in part via inhibiting PKC-α- and Nox-related signaling.

Self-Assembled Chiral Gold Supramolecules with Efficient Laser Absorption for Enantiospecific Recognition of Carnitine.

Stereospecific recognition of chiral molecules is ubiquitous in chemical and biological systems, thus leading to strong demand for the development of enantiomeric drugs, enantioselective sensors, and asymmetric catalysts. In this study, we demonstrate the ratio of d-Cys and l-Cys playing an important role in determining the optical properties and the structures of self-assembled Cys-Au(I) supramolecules prepared through a simple reaction of tetrachloroaurate(III) with chiral cysteine (Cys). The irregularly shaped -[d-Cys-Au(I)] n- or - [l-Cys-Au(I)] n- supramolecules with a size larger than 500 nm possessing strong absorption in the near-UV region and chiroptical characteristics were only obtained from the reaction of Au(III) with d-Cys or l-Cys. On the other hand, spindle-shaped -[d/l-Cys-Au(I)] n- supramolecules were formed when using Au(III) with mixtures of d/l-Cys. Our results have suggested that Au(I)···Au(I) aurophilic interactions, and stacked hydrogen bonding and zwitterionic interactions between d/l-Cys ligands are important in determining their structures. The NaBH4-mediated reduction induces the formation of photoluminescent gold nanoclusters (Au NCs) embedded in the chiral -[d-Cys-Au(I)] n- or -[l-Cys-Au(I)] n- supramolecules with a quantum yield of ca. 10%. The as-formed Au NCs/-[d-Cys-Au(I)] n- and Au NCs/-[l-Cys-Au(I)] n- are an enantiospecific substrate that can trap l-carnitine and d-carnitine, respectively, and function as a nanomatrix for surface-assisted laser desorption/ionization mass spectrometry (LDI-MS). The high absorption efficiency of laser energy, analyte-binding capacity, and homogeneity of the Au NCs/-[Cys-Au(I)] n- allow for quantitation of enantiomeric carnitine down to the micromolar regime with high reproducibility. The superior efficiency of the Au NCs/-[d-Cys-Au(I)] n- substrate has been further validated by quantification of l-carnitine in dietary supplements with accuracy and precision. Our study has opened a new avenue for chiral quantitation of various analytes through LDI-MS using metal nanocomposites consisting of NCs and metal-ligand complexes.

Ginger Phytochemicals Inhibit Cell Growth and Modulate Drug Resistance Factors in Docetaxel Resistant Prostate Cancer Cell.

Ginger has many bioactive compounds with pharmacological activities. However, few studies are known about these bioactive compounds activity in chemoresistant cells. The aim of the present study was to investigate the anticancer properties of ginger phytochemicals in docetaxel-resistant human prostate cancer cells in vitro. In this study, we isolated 6-gingerol, 10-gingerol, 4-shogaol, 6-shogaol, 10-shogaol, and 6-dehydrogingerdione from ginger. Further, the antiproliferation activity of these compounds was examined in docetaxel-resistant (PC3R) and sensitive (PC3) human prostate cancer cell lines. 6-gingerol, 10-gingerol, 6-shogaol, and 10-shogaol at the concentration of 100 µM significantly inhibited the proliferation in PC3R but 6-gingerol, 6-shogaol, and 10-shogaol displayed similar activity in PC3. The protein expression of multidrug resistance associated protein 1 (MRP1) and glutathione-S-transferase (GSTπ) is higher in PC3R than in PC3. In summary, we isolated the bioactive compounds from ginger. Our results showed that 6-gingerol, 10-gingerol, 6-shogaol, and 10-shogaol inhibit the proliferation of PC3R cells through the downregulation of MRP1 and GSTπ protein expression.

The water extract of Liuwei dihuang possesses multi-protective properties on neurons and muscle tissue against deficiency of survival motor neuron protein.

BACKGROUND: Deficiency of survival motor neuron (SMN) protein, which is encoded by the SMN1 and SMN2 genes, induces widespread splicing defects mainly in spinal motor neurons, and leads to spinal muscular atrophy (SMA). Currently, there is no effective treatment for SMA. Liuwei dihuang (LWDH), a traditional Chinese herbal formula, possesses multiple therapeutic benefits against various diseases via modulation of the nervous, immune and endocrine systems. Previously, we demonstrated water extract of LWDH (LWDH-WE) protects dopaminergic neurons and improves motor activity in models of Parkinson's disease. PURPOSE: This study aimed to investigate the potential protection of LWDH-WE on SMN deficiency-induced neurodegeneration and muscle weakness. STUDY DESIGN: The effects of LWDH-WE on SMN deficiency-induced neurotoxicity and muscle atrophy were examined by using SMN-deficient NSC34 motor neuron-like cells and SMA-like mice, respectively. METHODS: Inducible SMN-knockdown NSC34 motor neuron-like cells were used to mimic SMN-deficient condition. Doxycycline (1 µg/ml) was used to induce SMN deficiency in stable NSC34 cell line carrying SMN-specific shRNA. SMAΔ7 mice were used as a severe type of SMA mouse model. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays. Apoptotic cells and neurite length were observed by inverted microscope. Protein expressions were examined by western blots. Muscle strength of animals was evaluated by hind-limb suspension test. RESULTS: LWDH-WE significantly increased SMN protein level, mitochondrial membrane potential and cell viability of SMN-deficient NSC34 cells. LWDH-WE attenuated SMN deficiency-induced down-regulation of B-cell lymphoma-2 (Bcl-2) and up-regulation of cytosolic cytochrome c and cleaved caspase-3. Moreover, LWDH-WE prevented SMN deficiency-induced inhibition of neurite outgrowth and activation of Ras homolog gene family, member A (RhoA)/ Rho-associated protein kinase (ROCK2)/ phospho-LIM kinase (p-LIMK)/ phospho-cofilin (p-cofilin) pathway. Furthermore, in SMA-like mice, LWDH-WE improved muscle strength and body weight accompanied with up-regulation of SMN protein in spinal cord, brain, and gastrocnemius muscle tissues. CONCLUSION: The present study demonstrated that LWDH-WE protects motor neurons against SMN deficiency-induced neurodegeneration, and it also improves the muscle strength of SMA-like mice, suggesting the potential benefits of LWDH-WE as a complementary prescription for SMN deficiency-related diseases.

Preliminary physician and pharmacist survey of the National Health Insurance PharmaCloud system in Taiwan.

BACKGROUND: The PharmaCloud system, a cloud-based medication system, was launched by the Taiwan National Health Insurance Administration (NHIA) in 2013 to integrate patients' medication lists among different medical institutions. The aim of the preliminary study was to evaluate satisfaction with this system among physicians and pharmacists at the early stage of system implementation. METHODS: A questionnaire was developed through a review of the literature and discussion in 6 focus groups to understand the level of satisfaction, attitudes, and intentions of physicians and pharmacists using the PharmaCloud system. It was then administered nationally in Taiwan in July to September 2015. Descriptive statistics and multiple regression were performed to identify variables influencing satisfaction and intention to use the system. RESULTS: In total, 895 pharmacist and 105 physician questionnaires were valid for analysis. The results showed that satisfaction with system quality warranted improvement. Positive attitudes toward medication reconciliation among physicians and pharmacists, which were significant predictors of the intention to use the system (ß= 0.223, p < 0.001). Most physicians and pharmacists agreed that obtaining signed patient consent was needed but preferred that it be conducted by the NHIA rather than by individual medical institutions (4.02 ± 1.19 vs. 3.49 ± 1.40, p < 0.01). CONCLUSIONS: The preliminary study results indicated a moderate satisfaction toward the PharmaCloud system. Hospital pharmacists had a high satisfaction rate, but neither are physicians and community pharmacists. Continuously improvement on system quality has been performing based on the results of this preliminary survey. Policies and standardization processes, including privacy protection, are still warranted further actions to make the Taiwan PharmaCloud system a convenient platform for medication reconciliation.

Photothermal therapeutic response of cancer cells to aptamer-gold nanoparticle-hybridized graphene oxide under NIR illumination.

The objective of this study was to synthesize a nanocomposite, aptamer-gold nanoparticle-hybridized graphene oxide (Apt-AuNP-GO), to facilitate targeted treatment of tumor cells by near-infrared (NIR) light-activatable photothermal therapy. We also investigated whether Apt-AuNP-GO with NIR illumination modulates heat shock proteins (HSPs) expression leading to therapeutic response in human breast cancer cells. These findings can provide strategies for improving the photothermal therapy efficacy of cancer. The self-assembled Apt-AuNP-GO nanocomposite could selectively target MUC1-positive human breast cancer cells (MCF-7) due to the specific interaction between the MUC1-binding-aptamer and the MUC1 (type I transmembrane mucin glycoprotein) on cell membrane. In addition, Apt-AuNP-GO has a high light-to-heat conversion capability for photoabsorption of NIR light, and it is able to exert therapeutic effects on MCF-7 cells at an ultralow concentration without inducing adverse effects in healthy cells. The Apt-AuNP-GO nanocomposites combine the advantages of GOs, AuNPs, and Apts, possess specific targeting capability, excellent biocompatibility, and tumor cell destruction ability, suggesting great potential for application in the photothermal therapy of breast cancer. Under NIR illumination, Apt-AuNP-GO induced transient increase in HSP70 expression, which decreased thereafter. This phenomenon may cause irreversible damage to Apt-AuNP-GO-treated MCF-7 cell under NIR illumination. We also demonstrated that the combination therapy of heat and HSP70 inhibitor could synergistically generate marked tumoricidal effects against breast cancer. These results suggest that the degree and duration of HSP70 protein expression are correlated with therapeutic effects against breast cancer for Apt-AuNP-GO-assisted photothermal therapy. We believe that such a nanocomposite can be readily extended to the construction of HSP70 inhibitors-loaded Apt-AuNP-GO, which could deliver both heat and HSP70 inhibitors to tumorigenic regions for the chemo-photothermal therapy.

Physician and consumer acceptance of the traditional chinese medicine clinical practice support system (TCMCPSS).

Although ICT-enabled clinical practices have been widely accepted by the Western medical society, informatics applications for traditional Chinese medicine (TCM) are under developed. An integrated traditional Chinese medicine clinical practice support system (TCMCPSS) has been developed to enhance data integration automation and treatment planning decision support of clinical practice of TCM. The acceptance of TCMCPSS had been assessed by 26 TCM physicians based on information clarity, clinical relevancy, and theoretical relevancy through a survey questionnaire using the 5-points Likert Scale. The average acceptance rate was 3.76. One hundred and fifty-four participants were recruited for the TCMCPSS feasibility study and reported the acceptance rate of 90%. The results indicated that while consumers were ready to embrace TCM practice assisted by informatics technologies, TCM physicians concerned more about the usefulness of the system and preserved caution to adopt TCMCPSS.

The Chinese herbal formula Liuwei dihuang protects dopaminergic neurons against Parkinson's toxin through enhancing antioxidative defense and preventing apoptotic death.

Liuwei dihuang (LWDH), a widely used traditional Chinese medicine (TCM), has been employed as an anti-aging prescription to improve declined function. Parkinson's disease (PD) is a common adult-onset neurodegenerative disorder characterized by the degeneration of dopaminergic nigrostriatal neurons with complex pathological mechanisms, including oxidative stress. Increasing evidence indicate that TCM has the potential to be neuroprotective drugs because of their antioxidant characteristics. The aim of this study is to investigate the mechanisms of LWDH-mediated protection in Parkinson's toxin-induced dopaminergic neurodegeneration by evaluating water extract of LWDH (LWDH-WE) in 1-methyl-4-phenylpyridinium (MPP(+))-treated primary mesencephalic neurons and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated C57BL/6 mice. In the present study, chemical profiling and quantitative analysis of LWDH-WE were revealed using 3D-HPLC technique, and were confirmed by the data of three batches of LWDH-WE. In primary mesencephalic neuronal cultures, LWDH-WE decreased MPP(+)-induced loss of tyrosine hydroxylase (TH)-positive neurons and increase of Annexin V-positive neurons. LWDH-WE reduced MPP(+)-induced oxidative damage via increasing antioxidant defense (SOD, GSH), decreasing ROS production, and down-regulating NADPH oxidases (Nox2 and Nox4). Also, LWDH-WE inhibited neuronal apoptosis by improving mitochondrial membrane potential, increasing antiapoptotic protein Bcl-2 expression, and down-regulating apoptotic signaling (Bax, cytochrome c, cleaved-caspase-3) in MPP(+)-treated neurons. In MPTP-treated C57BL/6 mice, LWDH-WE attenuated TH-positive neuronal loss in substantia nigra pars compacta (SNpc), and improved locomotor activity of mice. In conclusion, the present results reveal that LWDH-WE possesses protection on dopaminergic neurons through enhancing antioxidant defense and decreasing apoptotic death, suggesting the potential benefits of LWDH-WE for PD treatment.

Neuroprotective Effects of San-Huang-Xie-Xin-Tang in the MPP(+)/MPTP Models of Parkinson's Disease In Vitro and In Vivo.

San-Huang-Xie-Xin-Tang (SHXT), composed of Coptidis rhizoma, Scutellariae radix, and Rhei rhizoma, is a traditional Chinese medicine used for complementary and alternative therapy of cardiovascular and neurodegenerative diseases via its anti-inflammatory and antioxidative effects. The aim of this study is to investigate the protective effects of SHXT in the 1-methyl-4-phenylpyridinium (MPP(+))/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease. Rat primary mesencephalic neurons and mouse Parkinson disease model were used in this study. Oxidative stress was induced by MPP(+) in vitro and MPTP in vivo. In MPP(+)-treated mesencephalic neuron cultures, SHXT significantly increased the numbers of TH-positive neurons. SHXT reduced apoptotic signals (cytochrome and caspase) and apoptotic death. MPP(+)-induced gp91(phox) activation and ROS production were attenuated by SHXT. In addition, SHXT increased the levels of GSH and SOD in MPP(+)-treated neurons. In MPTP animal model, SHXT markedly increased TH-positive neurons in the substantia nigra pars compacta (SNpc) and improved motor activity of mice. In conclusion, the present results reveal the evidence that SHXT possesses beneficial protection against MPTP-induced neurotoxicity in this model of Parkinson's disease via its antioxidative and antiapoptotic effects. SHXT might be a potentially alternative and complementary medicine for neuroprotection.